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B J Day

Publications and source records attributed to B J Day.

44 records · Page 3Linked to original sources
PubMed1992

Potentiation of bromobenzene-induced pneumotoxicity by phenobarbital as determined by bronchoalveolar lavage fluid analysis.

Bromobenzene produces pulmonary, renal and hepatic damage in the rat. Phenobarbital potentiates bromobenzene-induced hepatotoxicity. Studies were initiated to determine if phenobarbital potentiates the pulmonary damage produced by bromobenzene. In a dose ranging study, adult male rats were treated daily for 4 days with phenobarbital (80 mg/kg, ip) and on the fifth day were dosed with 0, 2, 3, or 4 mmoles/kg, ip, bromobenzene. In a larger study phenobarbital was given for 4 days (80 mg/kg, ip), and bromobenzene (3.3 mmoles/kg, ip) was given on the fifth day. Pulmonary damage was assessed 24 hours later in the first study and 12 hours later in the second study by bronchoalveolar lavage fluid analysis (BALF), microsomal mixed function oxidase measurements and histopathological evaluations. BALF biochemical markers employed were gamma-glutamyl transpeptidase (GGT), lactate dehydrogenase (LDH) and total protein. Phenobarbital treatment greatly enhanced bromobenzene-induced GGT and LDH release into the lavage fluid in a dose-dependent manner. Phenobarbital treatment increased microsomal 7-O-dealkylation of both ethoxy- and pentoxyresorufin in the liver without affecting these activities in the lung. Bromobenzene treatment decreased the hepatic microsomal dealkylation of decreased the hepatic microsomal dealkylation of pentoxyresorufin in a dose-dependent manner. Since known rat pulmonary P450 isozymes have been reported to be insensitive to phenobarbital induction, it may be that the toxicity is due to transport of a reactive metabolite(s) formed in the liver to the lung or bromobenzene is activated by some other pulmonary P450 isozyme responsive to phenobarbital.

Analysis of Variance↗
PubMed1992

Effect of p-xylene metabolites, p-methylbenzyl alcohol and 2,5-dimethylphenol, on rat hepatic and pulmonary microsomal metabolism.

Pulmonary metabolites of p-xylene, p-methylbenzyl alcohol (PMBA) and 2,5-dimethylphenol (DMP), were employed to investigate the divergent effects of p-xylene on pulmonary and hepatic metabolism. Rats were given PMBA, DMP, or 10% cremophore (control) ip daily for 3 days, and effects on hepatic and pulmonary microsomal metabolism were determined 12 hours later. Both PMBA and DMP mimic the decrease in pulmonary benzyloxyresorufin-O-debenzylase activity previously reported for p-xylene, but neither could account for the potent induction of cytochrome P450 in the liver. Only PMBA had a consistent effect on P450IIB apoprotein levels, decreasing them in both the liver and lung. These data suggest that PMBA may have a significant role in the inhibition of pulmonary P450 caused by p-xylene.

Animals↗
PubMed1991

Hemispheric threshold differences for motor evoked potentials produced by magnetic coil stimulation.

A brief monophasic pulse through an electromagnetic coil preferentially activates motor pathways of each hemisphere, depending on the direction of coil current flow. Using the preferred direction for each hemisphere, the minimum stimulus intensity (threshold) that evoked compound muscle action potentials in the contralateral abductor digiti minimi (ADM) muscle was significantly less for the left hemisphere than the right. Threshold for biceps on each side was significantly higher than ADM, but there was no side-to-side difference. Assessing handedness using a standard handedness index, those who had less tendency to use the right hand for everyday tasks had greater differences between hemispheres for ADM thresholds. The lower threshold of the left-hemisphere projection to hand muscles is probably related to the asymmetry of corticomotoneuronal monosynaptic connections; a greater number project to the motor neuron pool of the right- than left-hand muscles.

Action Potentials↗
PubMed1990

gamma-Glutamyltranspeptidase in rat bronchoalveolar lavage fluid as a probe of 4-ipomeanol and alpha-naphthylthiourea-induced pneumotoxicity.

Bronchoalveolar lavage fluid analysis has gained popularity as a rapid in vivo screen to evaluate the toxicity of both systemic and inhaled pneumotoxicants and is used in addition to the more commonly evaluated pathologic changes. This study evaluated gamma-glutamyltranspeptidase (GGT) in the bronchoalveolar lavage fluid (BALF) along with the more commonly measured enzyme, lactate dehydrogenase (LDH), as a useful indicator of acute lung injury from systematically administered pneumotoxicants. Adult male rats were injected ip with 2, 3, or 3.5 mg/kg body weight of alpha-naphthylthiourea (ANTU) or 5, 10, or 20 mg/kg of 4-ipomeanol, and measurements were made 8 or 24 hr postdose, respectively. ANTU, which selectively damages pulmonary endothelial cells, caused extensive pleural effusions with striking increases in BALF protein and white blood cell (WBC) content. 4-Ipomeanol, which selectively damages nonciliated bronchiolar Clara cells, caused dose dependent increases in both GGT and LDH activities in the BALF with GGT being increased at all doses tested. BALF protein content was also increased in the 4-ipomeanol-treated groups, but this change was not dose dependent. Analysis of GGT in BALF was a sensitive method to assess cytotoxicity associated with 4-ipomeanol-induced injury but was less useful in monitoring pulmonary endothelial cell damage induced by ANTU. Measurements of BALF protein and WBC content proved to be better in assessing injury by agents such as ANTU that primarily affect vascular permeability.

Animals↗
PubMed1990

Kinetic comparison of rat pulmonary and renal gamma-glutamyl transpeptidase activities.

Glutathione (GSH) protects the lung against oxidative injury from environmental pollutants. gamma-Glutamyl transpeptidase (GGT) plays an integral role in the utilization and degradation of glutathione. Although GGT has been extensively studied in the kidney, little is known about GGT activity in the lung. This study compares pulmonary and renal GGT activities using L-gamma-glutamyl-p-nitroanilide as the substrate. The apparent Km values of pulmonary and renal GGTs were not significantly different. The pulmonary apparent maximum velocity was several orders of magnitude lower than that of the kidney. Inhibition studies, employing L-serine in the presence of 20 microM borate, revealed similar apparent Ki values. Pulmonary GGT behaves similar to renal GGT in respect to its affinity for substrates and inhibitors but has significantly less activity on a gram protein basis.

Animals↗
PubMedDate not supplied

Emetine myopathy in a patient with an eating disorder.

OBJECTIVE: To alert physicians to the dangers of a readily available, non-prescription drug by describing the clinical and pathological features of myopathy due to chronic poisoning with ipecac syrup in a patient with an eating disorder. CLINICAL FEATURES: A 27-year-old woman presented in 1991 with a right foot drop, followed a few months later by progressive severe neck and limb weakness associated with dysphagia, faecal incontinence and diffuse body ache. It emerged that she had been consuming increasing quantities of ipecac syrup (up to 200 mL per week) for three months to induce vomiting and weight loss. The serum creatine kinase activity was slightly elevated and electromyographic examination results were in keeping with a necrotising proximal myopathic process. Muscle biopsy showed vacuolar degeneration with myofibrilolysis and fine cytoplasmic body formation, consistent with a diagnosis of emetine myopathy. INTERVENTION AND OUTCOME: The patient was advised to stop taking ipecac and observed for the next few months. The symptoms resolved gradually and strength returned to normal in four months. CONCLUSION: Chronic emetine toxicity, with its potentially catastrophic consequences, should be remembered in the evaluation of neuromuscular symptoms in young women, in whom eating disorders are common and often unrecognised.

Adult↗